Unit 4 Asma Decompression Physiology

Front 1

Describe the primary purpose for aircraft cabin pressurization.

Back 1

To allow aircrew to perform work / carry out operational duties above the “physiological zone” (i.e., sea level to 10K’), and to provide protection against the physiological problems that can result to exposure to pressures outside the physiological zone.

Front 2

Name 6 advatages of cabin pressurization

Back 2

(1)         Reduced need to supplemental O2 (except for TACAIR aircraft)
(2)         Incidence of GI trapped gas pains is reduced
(3)         Cabin temp., humidity, & ventilation can be controlled w/in desired comfort levels
(4)         Crew & PAX in large ACFT can move about freely in a comfortable environment unencumbered by O2 masks or other life support equipment
(5)         Prolonged PAX flights, air evacuation, & troop mvt. can be accomplished with a minimum of fatigue & discomfort
(6)         Protection against middle ear & sinus pain by allowing cabin pressure to rise slowly in a controlled manner during descent from high altitudes

Front 3

Name 6 disadvantages of cabon pressurization

Back 3

(1)         Increased structural wt. & strength of the pressurized area to maintain structural integrity
(2)         Additional equipment & power requirements to support the pressurization, ventilation, & AC systems
(3)         ACFT max. performance & payload capacity is reduced due to added wt.
(4)         Additional maintenance & upkeep
(5)         Possible contamination of cabin air from smoke, fumes, CO, CO2, & odors
(6)         If a rapid decompression occurs à hypoxia, DCS, trapped gas expansion injuries, hypothermia, & cyclonic winds

Front 4

Describe the physical indications of a rapid decompression.

Back 4

Noise: caused by collision of two different air masses; can range from a “swishing” sound to a loud explosive sound
Fogging: (air at any temp. & pressure can hold only so much water vapor; sudden changes in temp. or pressure, or both, change the amount of water vapor the air can hold)
Temperature: (ambient temp. decreases w. increase in altitude);
Flying Debris: from unsecured objects that get caught up in the rapid rush / outflow of air from a pressurizedcabin, “cyclonic winds”

Hint 4

4

Front 5

Why does fogging occur during a rapid decompression?

Back 5

During a rapid decompression, temp. & pressure are reduced,reducing the holding capacity of air for water vapor;water vapor condenses out as fog

Front 6

Describe 4 factors that can affect the rate of a cabin pressurization.

Back 6

(1)         Cabin Volume: decompression time with a larger cabin volume will be slower than with a cabin of smaller volume
(2)         Size of the Opening: proportionality of cabin volume & cross-sectional area of the opening
(3)         Pressure Ratio: between the pressure w/in the cabin & the outside ambient pressure; the greater the ratio, the time for the air to escape will also increase, with the end result of a greater decompression time
(4)         Pressure Differential: the difference betw. the internal & external pressures will influence both the rate & severity of the decompression; the larger the pressure differential, the more severe the rapid decompression

Front 7

Relate the rate of cabin pressurization to respiratory related disorders.

Back 7

Respiratory: the lungs are potentially the most vulnerable part of the body during a rapid decompression (RD); if a rapid decompression is faster than the inherent capability of the lungs to decompress, a transient positive pressure builds up in the lungs.
If the escape of the air is blocked, or seriously impeded during the RD, the intrapulmonary pressure can build up high enough to cause tears or ruptures of the lung tissues & capillaries.

Front 8

Relate the rate of cabin pressurization to trapped gas related disorders.

Back 8

Ears & Sinuses: a RD is unlikely to cause symptoms in the middle ear or sinuses other than a strong “pop” felt in the ear (gas volume is expanding, bowing the tympanic membrane out, but also forcing air out the Eustachian Tube)
GI Tract Gas: a RD will cause a rapid expansion of trapped gas in the GI tract, with the potential for considerable abdominal distress.

Front 9

How can rapid decompression affect the vasovagal response?

Back 9

The diaphragm may be displaced upward by expansion of trapped gas in the stomach, which can retard respiratory movements. Distension of abdominal organs may stimulate the abdominal branches of the Vagus Nerve, resulting in cardiovascular depression (i.e., vasovagal response), and if severe enough, cause reduction in blood pressure, unconsciousness, and shock.

Front 10

Relate the rate of cabin pressurization to evolved gas related disorders.

Back 10

Evolved Gas Disorders (i.e., DCS): usually does not occur unless cabin altitude exceeds 18K’, and even then the incidence is small unless the cabin altitude reaches 25K’ to 30K’

Front 11

Compare the relative effects of depressurization on wet and dry gases.

Back 11

Over a given pressure reduction, wet gases expand to a greater degree (~2.5X ?) than dry gases due to the additional water vapor

Front 12

Gas in the GI tract is saturated with what which is related to what?

Back 12

water vapor, the partial pressure of which is related to body temp.

Front 13

Is water vapor in the GI tract relatively constant or not and why?

Back 13

B/c body temp. is relatively constant (37o C), the partial pressure of the water vapor is also constant at 47 mm Hg.

Front 14

What must you account for in determining the mechanical effects of gas expansion?

Back 14

In determining the mechanical effects of gas expansion, you must account for the non-compressibility of water vapor.

Front 15

State the anatomical structures most likely to be affected by a decrease / increase in ambient pressure.

Back 15

Ears (middle ear in particular)
Sinuses (especially frontal and maxillary)
Teeth (barodontalgia)Gastrointestinal (GI) Tract

Front 16

Describe the Eustachian tube

Back 16

Eustachian Tube {auditory tube}: 37 mm long {1.5”}, links the middle ear to the pharynx. Tympanic end is bony and usually open, whereas the pharyngeal end is cartilaginous, slit-like, and closed, acting like a one-way flutter valve

Front 17

Can ear blocks occur on ascent or descent? Why?

Back 17

Ear blocks can occur on ascent or descent when middle ear air pressure is unable to equalize with ambient air pressure. Normally occurs b/c the lower orifice of the Eustachian tube fails to function adequately, or it is swollen shut from a cold or ear infection

Front 18

Describe the physical, anatomical, and physiological causes of an ear block on both ascent.

Back 18

Ascent: ear blocks are less common b/c increasing middle ear pressure (relative to decreasing ambient pressure) forces open the “flutter valve” pharyngeal end of the Eustachian tube; contraction of the levator and tensor veli palatini muscles by yawning, chewing, and swallowing also helps to open the Eustachian tube.

Front 19

Describe the physical, anatomical, and physiological causes of an ear block on both descent.

Back 19

Descent (especially rapid descents from 15K’ to 5K’): ear blocks are more common b/c the collapsed, closed, pharyngeal end of the Eustachian tube prevents air from entering the tube, and the increasing negative pressure in the middle ear further holds the soft tissue together

Front 20

When must muscular (active) opening of the Eustachian tube via the Valsalva Maneuver must be accomplished and why?

Back 20

Before the differential pressure reaches 80-90 mm Hg; once this magnitude of pressure differential is reached, muscular action cannot overcome the suction effect on the closed Eustachian tube, and the tube is “locked.”

Front 21

Relative negative middle ear pressure does what 2 things?

Back 21

Retracts the tympanic membrane inward, and it also pulls on the delicate mucosal lining, leading to effusion (fluid collection) and hemorrhage w/in the middle ear.

Front 22

List the symptoms of an ear block.

Back 22

(1)         Pressure or pain
(2)         Muffled sound / hearing
(3)         Dizziness
(4)         Tinnitus (ringing in the ear)

Front 23

Describe the technique for prevention of ear blocks on ascent / descent.

Back 23

Ascent: yawn, chew, swallow; tense the throat muscles (levator and tensor veli palatine)
Descent: Valsalva Maneuver; ascend to relieve some of the pressure, attempt to self-clear via the Valsalva Maneuver, descend at a slower rate; politzerization

Front 24

Describe the sinuses

Back 24

* Sinuses: air-filled, relatively rigid, bony cavities lined with mucous membranes, connect with the nose by means of one or several small openings; if the openings are normal, air passes in/out of the cavities at the rate of ascent/descent, assuring adequate equalization of pressure.

Front 25

When do sinus blocks occur?

Back 25

Sinus blocks occur if the openings are obstructed by swelling of the mucous membrane lining (from infection or allergic reaction), polyps, or redundant tissue.

Front 26

Relative negative middle ear pressure does what 2 things?

Back 26

Retracts the tympanic membrane inward, and it also pulls on the delicate mucosal lining, leading to effusion (fluid collection) and hemorrhage w/in the middle ear.

Front 27

List the symptoms of an ear block.

Back 27

(1)         Pressure or pain
(2)         Muffled sound / hearing
(3)         Dizziness
(4)         Tinnitus (ringing in the ear)

Front 28

Describe the technique for prevention of ear blocks on ascent / descent.

Back 28

Ascent: yawn, chew, swallow; tense the throat muscles (levator and tensor veli palatine)
Descent: Valsalva Maneuver; ascend to relieve some of the pressure, attempt to self-clear via the Valsalva Maneuver, descend at a slower rate; politzerization

Front 29

Describe the sinuses

Back 29

* Sinuses: air-filled, relatively rigid, bony cavities lined with mucous membranes, connect with the nose by means of one or several small openings; if the openings are normal, air passes in/out of the cavities at the rate of ascent/descent, assuring adequate equalization of pressure.

Front 30

When do sinus blocks occur?

Back 30

Sinus blocks occur if the openings are obstructed by swelling of the mucous membrane lining (from infection or allergic reaction), polyps, or redundant tissue.

Front 31

Describe the physical, anatomical, and physiological causes of a sinus block.

Back 31

Sinus blocks can occur on ascent or descent, but are 90% more likely on descent (during ascent, expanding air usually forces it way out past the obstruction). During descent, pressure in the obstructed sinus is less than the surrounding (gradually increasing) ambient pressure, creating a vacuum effect on the delicate, thin, mucosal lining, resulting in severe pain. Some fluid may be drawn into the cavity, but a more serious complication is a pulling away of the mucosal lining with concomitant bleeding.

Front 32

The majority (name percentage) of sinus blocks involves which sinus cavity and why?

Back 32

70% of all sinus blocks involve the frontal sinus, and the chief cause is flying with a cold or congestion

Front 33

List the steps for treating a sinus block.

Back 33

DURING DESCENT
(1)         Level off and attempt to self-clear using the Valsalva Maneuver; if unsuccessful, ascend to relieve some of the pressure and Valsalva again
(2)         Use nasal spray and Valsalva again
(3)         Continue descent at a much slower rate, continue to perform the Valsalva Maneuver

Front 34

Describe the physical, anatomical of baro-induced tooth pain.

Back 34

* Tooth pain (barodontalgia): usually occurs on ascent only, especially btwn. 5K’ – 15K’. The pain may or may not become more severe with an increase in altitude. Pain is usually relieved on descent, an important feature which helps to distinguish it from pain in the upper jaw due to maxillary barosinusitis.

Front 35

Describe the physiological causes of barodontalgia

Back 35

Causes: some sort of pre-existing dental pathology, completely
normal teeth are not effected
(1)         Gum abscess – dull pain on ascent
(2)         Root abscess – dull pain on ascent
(3)         Inflamed pulp (pulpitis) / carious teeth – sharp pain on ascent (from decay or recent dental work)
(4)         Imperfect fillings

Front 36

List the steps for treatment of tooth pain.

Back 36

Descend immediately, report to dental for check-up / repair of dental work

Front 37

When does GI trapped gas pain usually begin and why?

Back 37

Pain & discomfort usually starts at altitudes above 18K’ (altitude at which ambient pressure is 1/2 the earth’s atmosphere, gas has expanded to 2X its normal volume at sea level; also, wet gases expand to a greater volume than dry gases due to additional water vapor). Above 25K’, gas distension may produce severe pain

Front 38

State Henry's Law

Back 38

* Henry’s Law: amount of gas dissolved in solution varies directly with the partial pressure of that gas over the solution

Front 39

List some causes/sources of trapped GI gas

Back 39

Causes/ Sources of Trapped Gas:
(1)         Swallowed air (drinking, especially drinking carbonated beverages) and chewing gum
(2)         Gas formed as a result of digestion, fermentation, bacterial decomposition, etc.; diet (gas=producing foods)

Front 40

List the steps for treatment of trapped gas expansion in the intestines.

Back 40

Treatment:
(1)         Vent the gas! Belching or passing gas (“Waste it or taste it”)
(2)         Ball up the hand into a fist & massage abdomen from right to left, attempt to break up big bubbles into smaller bubbles that are easier to pass

Front 41

When a physiologically inert gas like N2 is inhaled, what happens to that gas after inhalation?

Back 41

When a physiologically inert gas (such as N2, that is not involved in oxidative metabolism & is not “used” by the body) is inhaled, the gas dissolves in the body until it reaches equilibrium with the liquid phase (blood & tissue) – saturation. The [N2] dissolved is proportional to the partial pressure of N2 in the inhaled gas

Front 42

State the effects of atmospheric pressure on the incidence of DCS.

Back 42

The decrease in ambient pressure with an increase in altitude causes a reduction in the N2 partial pressure, setting up a pressure gradient in the lungs - supersaturation, N2 off-gases from the tissues, dissolves in the blood and is carried to the lungs to be exhaled
If too much N2 off-gases too rapidly, micro-bubbles grow and form larger bubbles (critical supersaturation) that may block veins and arteries (DCS).

Front 43

What altitude is DCS most likely to occur

Back 43

DCS more likely to occur with exposure to altitudes of 18K’ and above

Front 44

Micro-bubble nuclei are believed to be generated by what?

Back 44

* Micro-bubble nuclei are believed to be generated by motion (and other factors such as supersaturation); seems to be a dynamic equilibrium btwn. generation and destruction in the tissues

Front 45

How do "seed" bubbles come into play with DCS?

Back 45

“Seed” bubbles may already be present in the blood when decompression occurs; combined with the effects of supersaturation, these “seed” bubbles may enlarge to the point where clinical manifestation of DCS occurs supersaturation

Front 46

Describe the relationship between micro-bubble nuclei and DCS.

Back 46

* Micro-bubble nuclei form in areas of negative hydrostatic pressure:
(1) Areas of turbulent blood flow (small vortices in the bloodstream)
(2) Viscous adhesion (negative pressure generated in a liquid btwn. two moving surfaces {e.g., shearing joints, vacuum phenomena in joints leading to the cracking” of joints}); require a pressure differential of only fractions of an atmosphere
(3) Negative pressure pockets btwn. working muscles
(4) N2 bubble adhesion to surface proteins on cell layers

Front 47

What is supersaturation (in regard to gases and DCS)

Back 47

Supersaturation: results when inert gas tension (PN2) exceeds ambient barometric pressure (PB)

Front 48

If the decompression exceeds some critical rate for the body to off-gas N2 what happens?

Back 48

If the decompression exceeds some critical rate for the body to off-gas / eliminate N2, the tissues and blood become supersaturated with N2 and bubbles may form

Front 49

What can supersatuiration occur from in regard to N2.

Back 49

Supersaturation may also occur from negative pressures generated during many mechanical processes, resulting in a local reduction of absolute pressure in a liquid system
(1)         Flow of a liquid through a local narrowing in a tube results in a local drop of pressure (Bernoulli principle), which in turn can lead to transient bubble formation (Reynold’s cavitation)
(2)         Viscous adhesion – negative pressures generated when two surfaces in a liquid are pulled apart; bubbles generated by this mechanism are said to be generated by tribonucleation

Front 50

What is critical supersaturation in regard to DCS?

Back 50

Critical supersaturation: occurs when a physiologically inert gas (N2) comes out of solution and forms bubbles
A level of supersaturation can be reached that the body can tolerate w/out the inert gas coming out of solution to form bubbles, but once a critical supersaturation ratio is reached bubbles develop that may lead to DCS

Front 51

Bubbles that can lead to DCS form where?

Back 51

Bubbles may form in blood, lymphatics, or tissue;

Front 52

Where is inert gas tension (i.e. N2) higher, capillary, venous blood and/or arterial blood?

Back 52

Capillary and venous blood

Front 53

Describe Haldane’s theory for DCS.

Back 53

Body can be represented by five (5) hypothetical body / tissue “compartments”, each of which absorbs and releases N2 at different rates (probably due to differing perfusion rates) known as “half-times” –half the time it takes for a dissolved gas in a tissue to equilibrate (either by up-take or elimination) to a new pressure, or to reach full saturation at a new pressure

Front 54

The rate of N2 gas uptake in the blood and elimination depends on:

Back 54

(1)         Gas concentration gradient btwn. blood and tissue
(2)         Tissue blood flow (perfusion)
(3)         Ratio of blood and tissue gas solubilities (e.g., N2 is 5X more soluble in fat than in water)

Front 55

Describe the importance of the 2:1 ratio of ambient pressure to tissue gas tension as it relates to DCS

Back 55

Body can tolerate a certain amount of excess inert gas (N2) with no apparent ill effects (tissues/blood can be supersaturated with N2 as a result of a decrease in PB, but N2 doesn’t bubble out of solution), as long as the ratio of ambient pressure (PB) to tissue gas tension (PN2) is 2:1 or less. If this ratio is exceeded (critical supersaturation), N2 begins to bubble out of solution

Front 56

What is Haldane's Ratio?

Back 56

Haldane’s 2:1 Ratio:
R = PN2/PB
(this is ambient pressure)

Front 57

Type I DCS are what % of all altitude DCS cases?

Back 57

Type I DCS: 85-90% of all altitude DCS cases

Front 58

Name the 2 tpes of Type I DCS

Back 58

Joint Pain/Bends and Cutaneous (Skin) bends

Front 59

List the symptoms of Joint paoin/Bends

Back 59

Joint Pain / “Bends” (60-70% of altitude DCS cases): – joint pain, especially in the upper extremities (shoulder, elbow); starts gradually as a mild discomfort that is difficult to localize (i.e., “niggles”); pain intensity gradually increases over time into a deep dull ache

Front 60

List the symptoms of cutaneous (skin) bends

Back 60

Cutaneous (Skin) Bends: itching (pruritis), creepy-crawly sensation (formication); mottling or marbling of the skin (Cutis Marmorata) is caused by venous obstruction by intravascular bubbles and usually precedes the more serious forms of DCS

Front 61

Type II DCS comprises what % of all altitude DCS cases?

Back 61

Type II DCS: 10-15% of all altitude DCS cases

Front 62

List the 2 types of Type II DCS

Back 62

Neurological and cardiopulmonary (Chokes)

Front 63

What are the 2 types of neurological DCS?

Back 63

peripheral/spinal and central/brain

Front 64

List the symptoms of peripheral/spinal DCS

Back 64

Peripheral / Spinal – burning or tingling sensation (paresthesias), numbness or weakness

Front 65

Peripheral/spinal DCSis more common in what types of pressure changing activities?

Back 65

More common in diving activities

Front 66

What percent of Type II DCS is mad up of peripheral/spinal altitude DCS?

Back 66

Accounts for < 10% of the Type II altitude DCS cases

Front 67

List the symptoms of central/brain DCS

Back 67

Central / Brain – most common form of Type II altitude DCS; headache, visual disturbances, hemiplegia, hemisensory loss, incordination, personality changes, confusion

Front 68

Bilateral limb pain, sharp, knife-like pain that “shoots” down an extremity or encircles the body trunk and/hips, and pain that “moves” from one area to another arises from the nervous system and is treated as what?

Back 68

Type II DCS

Front 69

List the symptoms of cardiopulmonary (Chokes) DCS

Back 69

Cardiopulmonary Symptoms (“Chokes”): very rare, but fatal; due to profuse pulmonary gas emboli impede respiratory gas exchange; burning substernal chest pain that is aggravated by breathing, cough, and shortness of breath (dyspnea)

Front 70

What contributes to bubble formationduring pressure changes?

Back 70

* Once bubbles form, they tend to expand as dissolved gases and continue to come out of solution. CO2, a highly diffusible gas, contributes to bubble enlargement, especially if formed in excess by vigorous exercise

Front 71

Bubbles have what 2 pathophysiological effects?

Back 71

(1)         Direct mechanical effects of bubbles may obstruct blood vessels or distort tissue, causing pain, ischemia, and infarction
(2)         Tissue-Bubble interface surface activity results in protein denaturation and platelet aggregation, causing endothelial damage

Front 72

List the steps for treating DCS.

Back 72

(1)         100% O2 using a well-fitted mask
(2)         Descend as low as safely possible
(3)         Recompression / hyperbaric chamber; if transportation is required, it must be at or near ground-level (in no case should cabin pressure altitude be more than 1,000 feet (305 m) than the pressure altitude at the point of embarkation)

Front 73

Describe 4 physical and physiological benefits of hyperbaric therapy in the treatment of DCS.

Back 73

(1)         Mechanical compression of gas bubbles
(2)         Elevation of PO2 in inspired air establishes a positive N2 gradient that reduces the size of the N2 bubbles and increases the rate of N2 elimination
(3)         Perfusion of ischemic tissues
(4)         Correction of local tissue hypoxia – disrupts the vicious cycle of hypoxia-induced tissue damage that causes tissue edema and interferes with circulation and oxygenation

Front 74

What are 4 potential causes for over-inflation injuries?

Back 74

Potential Causes for All Over-Inflation Injuries: need a sufficient pressure differential to over-inflate the lungs and rupture the alveoli
(1)         Breath hold during a rapid decompression
(2)         Breath hold on ascent while breathing compressed air (e.g., HABD bottle)
(3)         Repeated Valsalva maneuvers
(4)         Excessive coughing, sneezing, vomiting

Front 75

Describe the causes of pneumothorax

Back 75

Causes: lung-over-inflation, alveoli rupture, and air accumulates in the pleural cavity causing lung collapse

Front 76

Type II DCS comprises what % of all altitude DCS cases?

Back 76

Type II DCS: 10-15% of all altitude DCS cases

Front 77

List the 2 types of Type II DCS

Back 77

Neurological and cardiopulmonary (Chokes)

Front 78

What are the 2 types of neurological DCS?

Back 78

peripheral/spinal and central/brain

Front 79

List the symptoms of peripheral/spinal DCS

Back 79

Peripheral / Spinal – burning or tingling sensation (paresthesias), numbness or weakness

Front 80

Peripheral/spinal DCSis more common in what types of pressure changing activities?

Back 80

More common in diving activities

Front 81

Describe 13 factors which may
predispose a crewmember to DCS.

Back 81

(1)         Altitude Attained: incidence and severity of DCS increases with increasing altitude
(2)         Duration of Exposure: at all altitudes above 18K’ (5,44 m), the longer the duration of exposure, the greater the incidence of DCS
(3)         Previous Exposures to Altitude: a 2nd exposure to altitudes > 18K’ (5,488 m) following an exposure to such an altitude in the preceding 3 hours will greatly increase the chances of DCS occurring, even if the first exposure was asymptomatic
(4)         Flying Following Diving: 24-hour wait period after surfacing
(5)         Age: incidence of DCS increases with age; 3-fold increase in the incidence btwn. 19-25-yr-olds and 40-45-yr-olds; significantly greater risk in those older than 42
(6)         Gender: retrospective studies indicated a higher incidence in females than males, but more recent studies have not revealed any significant difference btwn. males and females
(7)         Exercise: mild and strenuous exercise both equally increase DCS incidence (altitude equivalent with exercise is an additional 3K’ to 5K’); probably due to increased muscle perfusion, an increase in inert gas uptake (i.e., increased respiration), shear forces in joints causing mico-bubbles, and increased CO2 which can accelerate bubble growth
(8)         Injury: no convincing evidence exists to associate previous injury with DCS, but the acute stages of an injury to a joint may increase the susceptibility to the “bends” b/c of perfusion changes associated with the injury/healing mechanisms
(9)         Body Build: long-time belief that obesity increases the susceptibility to DCS. Although it seems prudent to continue to accept this principle b/c of other known adverse effects of obesity, no scientific evidence validation exists to date
(10)    Temperature: very cold ambient temp. (-23oC) increases the risk of DCS perhaps by changes in N2 washout from peripheral vasoconstriction
(11)    Hypoxia: anecdotal evidence suggests an association btwn. hypoxia and DCS
(12)    Acid-Base Balance: elevated PCO2 levels are associated with severe “bends” (CO2 may contribute to bubble growth); deliberate hyperventilation at altitude decreases the pain associated with the “bends”
(13) Dehydration: causes the blood to thicken which inhibits blood circulation and this in turn reduces N2 elimination

Front 82

What is primary spontaneous pneumothorax and when does it occur?

Back 82

* Primary spontaneous pneumothorax – occurs without trauma, chest injury, or over-inflation; lung bleb (an imperfection in the lining of the lungs) bursts causing the lung to deflate

Front 83

Describe the symptoms of pneumothorax

Back 83

Symptoms: sudden, sharp chest pain, shortness of breath and cough

Front 84

Describe the causes of substernal emphysema (pneumomediastinum).

Back 84

Causes: lung-over-inflation, alveoli rupture, air accumulates in the mediastinum (space btwn. The lungs containing the heart and its large vessels, trachea, esophagus, etc.) and chest wall)

Front 85

Describe the symptoms of substernal emphysema (pneumomediastinum).

Back 85

Symptoms: “fullness” in the chest, or a dull ache / chest pain underneath the sternum, that may radiate to the neck and arms, pain may worsen with breathing and swallowing

Front 86

Describe the causes of an aero-embolism (arterial gas embolism).

Back 86

Causes: lung over-inflation forces air into the pulmonary arteries and veins, once the bubbles enter the arterial and venous circulation they can be dispersed throughout the body;

Front 87

How can death occur from an arterial gas embolism?

Back 87

Death can occur if a large bubble lodges in the heart, stopping blood flow from the right ventricle to the lungs (similar to vapor lock in engine fuel systems)

Front 88

What's more dangerous an arterial gas emboli or a venous gas emboli and why?

Back 88

Arterial gas emboli are more serious than venous emboli, b/c. a gas bubble in an artery may directly stop blood flow to an area/tissue fed by the artery

Front 89

Describe the symptoms of an aero-embolism (arterial gas embolism).

Back 89

Symptoms: sudden, dramatic, and life-threatening; LOC, dizziness, paralysis, weakness in the extremities, large areas of abnormal sensation, blurry vision, convulsions

Front 90

What treatment table is used to treat an arterial gas embolism?

Back 90

Table 6A

Front 91

Describe Treatment Table 6A including length of time

Back 91

Treatment Table 6A (5 hrs., 50 min.): similar to treatment table 6 (TT6), except patient is initially pressurized to a depth of 165 feet sea water (fsw) vice the TT6 depth of 60 fsw; massive amounts of air can be introduced into the cerebral circulation, so it’s necessary to mechanically compress the entrapped air maximally

Front 92

Describe the standard treatment protocol(s) for Aero-Embolism (Arterial Gas Embolism:

Back 92

Recompression / Hyperbaric Therapy using USN Dive Treatment Tables
(1)         Mechanical compression of bubbles using USN Div Treatment Table 6A
(2)         Hyperbaric oxygenation of tissues

Front 93

Describe the standard treatment protocol(s) for Pneumothorax and Substernal Empysema (Pneumomediastinum):

Back 93

“Small” over-inflation injuries may resolve on their own (i.e, the pleura reabsorb the air); for larger injuries, the air must be removed from around the lungs, either by aspiration, or by using a chest tube inserted btwn. The ribs to drain the air and allow the lung to re-expand.
* oxygen may be needed to help the ambient air surrounding the lungs to be reabsorbed more quickly. Recompression IS NOT indicated.